No matter if you live in a house or apartment or simply would like to ensure your home is free from EMFs There are plenty options to limit your exposure. One of the most effective is to reduce your electronic device use. You could also consider EMF block paint to prevent EMF radiation from entering your house. https://squareblogs.net/dancerbaboon9/information-about-emf-blocking-radiation to shield your home from EMF radiation is to put up a RF shielding canopy. This is a fabric made of net that has EMF shielding. https://te.legra.ph/EMF-Block-Paint-plus-EMF-Shielding-04-13 's used to block EMFs from entering a space. Another option is to have your home fitted with a conductive enclosure. These enclosures are known as Faraday cages.
A number of studies have proven how the non-ionizing energy of RF can cause antiproliferative properties in HCC cells. The mechanism behind AM RF EMF's anticancer activity in vitro is thought to involve down-regulation of cancer stem cells. This could be the reason for the long-term response seen in patients suffering from advanced HCC. However, the mechanism behind AM RF EMF's effect in patients with cancer is not clear.
https://ctxt.io/2/AACQWWaZEA on the effects of AM RF EMFs on HCC tumour growth in vivo was studied in mice. The tumours were divided into three groups. One group did not have exposure RF EMF. Another group of participants was subjected to RF EMF at a frequency that is similar to the one used by humans. In the third, they were subjected the RF EMF in HCC-specific frequencies. The effect of HCCMF on tumors was compared to that of RCF. The results indicated that tumours treated with HCCMF had significant shrinkage. However, the tumors treated with RCF did not show any evidence of tumour shrinkage.
The reason for tumour-specific AM RF EMF could be due to the fact that cancer cells require Cav3*2 T-type voltage calcium channels for their proliferation and down-regulation. AM RF EMF's antiproliferative effects upon HCC cells is mediated through CACNA1H, a protein which regulates the Ca2+ influx specific to tumors. The results suggest that CACNA1H could have wider implications for treatment and diagnosis of different cancers.
The tumours in the control group were not exposed to EMF from RF, and fed a normal diet of mice. The tumors of those in the HCCMF group were treated with Huh7 cells after they were 5 to 7 weeks old. The tumors were removed when they showed excessive burden.
The tumours from the three groups also displayed different growth curves. The tumours treated with HCCMF saw a significant reduction in the size of the tumour after eight weeks. However, the tumours that were treated using RCF did not show any shrinkage. The difference was highly significant. The tumours treated with RCF showed necrosis, which is common when tumors are exposed to RCF. It is possible that this necrosis was due to a lack of oxygen in the more invasive tumours.
In summary, the results show an AM-RF EMF has anticancer activity in vitro and in vivo. Numerous studies have demonstrated it is true that AM RF EMF produces measurable tumour shrinkage in HCC patients. There is a possibility that AM RF EMF causes these effects due to CACNA1H, a protein involved in the process of tissue-specific Ca2+ influx. In addition, AM RF EMF may cause a lasting effect on the development of HCC tumours in vivo.